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棕色挪威大鼠氯化汞性肾炎中自身抗体合成的自动调节。I. T抑制细胞的作用。

Autoregulation of autoantibody synthesis in mercuric chloride nephritis in the Brown Norway rat. I. A role for T suppressor cells.

作者信息

Bowman C, Mason D W, Pusey C D, Lockwood C M

出版信息

Eur J Immunol. 1984 May;14(5):464-70. doi: 10.1002/eji.1830140515.

DOI:10.1002/eji.1830140515
PMID:6233159
Abstract

Mercuric chloride injections in the Brown Norway rat induce the transient formation of anti-glomerular basement membrane (GBM) autoantibodies. Transfer of spleen cells from convalescent animals, after circulating anti-GBM autoantibodies are no longer detectable, inhibits reinduction of the disease by HgCl2 in naive recipients. This inhibition is significantly less when the T suppressor cell population is depleted by the monoclonal antibody, MRC OX8 , before transfer. Our studies suggest a role for T suppressor cells in autoregulation in this animal model of autoimmune nephritis and may form a basis for the design of specific therapy for anti-GBM disease in man.

摘要

给棕色挪威大鼠注射氯化汞会诱导抗肾小球基底膜（GBM）自身抗体的短暂形成。在循环中的抗GBM自身抗体不再可检测到之后，将恢复期动物的脾细胞转移到未患病的受体中，可抑制氯化汞对疾病的再次诱导。在转移前用单克隆抗体MRC OX8耗尽T抑制细胞群体时，这种抑制作用明显减弱。我们的研究表明T抑制细胞在这种自身免疫性肾炎动物模型的自身调节中起作用，并且可能为人类抗GBM疾病的特异性治疗设计奠定基础。

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